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You searched for +publisher:"Vanderbilt University" +contributor:("Aaron B. Bowman"). Showing records 1 – 8 of 8 total matches.

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Vanderbilt University

1. Tidball, Andrew Martin. A Manganese-Handling Deficit in Huntingtonâs Disease Selectively Impairs ATM-p53 Signaling.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 The essential micronutrient manganese is enriched in brain, especially the basal ganglia. We sought to identify neuronal signaling pathways responsive to neurologically relevant manganese levels,… (more)

Subjects/Keywords: manganese; induced-pluripotent stem cells; ATM; p53; cell signaling; cytotoxicity; genomic instability; Huntingtons disease

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APA (6th Edition):

Tidball, A. M. (2014). A Manganese-Handling Deficit in Huntingtonâs Disease Selectively Impairs ATM-p53 Signaling. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-09252014-134959/ ;

Chicago Manual of Style (16th Edition):

Tidball, Andrew Martin. “A Manganese-Handling Deficit in Huntingtonâs Disease Selectively Impairs ATM-p53 Signaling.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed December 07, 2019. http://etd.library.vanderbilt.edu/available/etd-09252014-134959/ ;.

MLA Handbook (7th Edition):

Tidball, Andrew Martin. “A Manganese-Handling Deficit in Huntingtonâs Disease Selectively Impairs ATM-p53 Signaling.” 2014. Web. 07 Dec 2019.

Vancouver:

Tidball AM. A Manganese-Handling Deficit in Huntingtonâs Disease Selectively Impairs ATM-p53 Signaling. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2019 Dec 07]. Available from: http://etd.library.vanderbilt.edu/available/etd-09252014-134959/ ;.

Council of Science Editors:

Tidball AM. A Manganese-Handling Deficit in Huntingtonâs Disease Selectively Impairs ATM-p53 Signaling. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://etd.library.vanderbilt.edu/available/etd-09252014-134959/ ;


Vanderbilt University

2. Vollbrecht, Peter John. A Role for Astrocytes in Dopamine-Glutamate Interactions of the Prefrontal Cortex.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Both dopamine and glutamate are critically involved in cognitive processes such as working memory. Evidence has demonstrated that manipulation of either neurotransmitter can lead to… (more)

Subjects/Keywords: Schizophrenia; EAAT2; GLT-1; Glutamate; Dopamine; Prefrontal Cortex

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APA (6th Edition):

Vollbrecht, P. J. (2014). A Role for Astrocytes in Dopamine-Glutamate Interactions of the Prefrontal Cortex. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-03242014-203500/ ;

Chicago Manual of Style (16th Edition):

Vollbrecht, Peter John. “A Role for Astrocytes in Dopamine-Glutamate Interactions of the Prefrontal Cortex.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed December 07, 2019. http://etd.library.vanderbilt.edu/available/etd-03242014-203500/ ;.

MLA Handbook (7th Edition):

Vollbrecht, Peter John. “A Role for Astrocytes in Dopamine-Glutamate Interactions of the Prefrontal Cortex.” 2014. Web. 07 Dec 2019.

Vancouver:

Vollbrecht PJ. A Role for Astrocytes in Dopamine-Glutamate Interactions of the Prefrontal Cortex. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2019 Dec 07]. Available from: http://etd.library.vanderbilt.edu/available/etd-03242014-203500/ ;.

Council of Science Editors:

Vollbrecht PJ. A Role for Astrocytes in Dopamine-Glutamate Interactions of the Prefrontal Cortex. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://etd.library.vanderbilt.edu/available/etd-03242014-203500/ ;


Vanderbilt University

3. Kumar, Kevin Krishan. Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Manganese (Mn) is both an essential biological cofactor and neurotoxicant. Disruption of Mn biology in the basal ganglia has been implicated in the pathogenesis of… (more)

Subjects/Keywords: High Throughput Screening; Manganese; Neurodegenerative diseases; Human Induced Pluripotent Stem Cells; Metabolomics

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APA (6th Edition):

Kumar, K. K. (2014). Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu//available/etd-08262014-111713/ ;

Chicago Manual of Style (16th Edition):

Kumar, Kevin Krishan. “Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed December 07, 2019. http://etd.library.vanderbilt.edu//available/etd-08262014-111713/ ;.

MLA Handbook (7th Edition):

Kumar, Kevin Krishan. “Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches.” 2014. Web. 07 Dec 2019.

Vancouver:

Kumar KK. Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2019 Dec 07]. Available from: http://etd.library.vanderbilt.edu//available/etd-08262014-111713/ ;.

Council of Science Editors:

Kumar KK. Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://etd.library.vanderbilt.edu//available/etd-08262014-111713/ ;


Vanderbilt University

4. Warren, Emily Booth. Mitochondrial dysfunction in the striatum: Implications for L-DOPA Induced Dyskinesia.

Degree: PhD, Pharmacology, 2018, Vanderbilt University

 L-DOPA Induced Dyskinesia (LID) is the motor complication involving an overproduction of movement that arises from L-DOPA treatment of Parkinson's disease (PD). Despite the high… (more)

Subjects/Keywords: mitochondria; parkinsons disease; l-dopa induced dyskinesia; striatum; mitochondrial DNA; ethidium bromide

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APA (6th Edition):

Warren, E. B. (2018). Mitochondrial dysfunction in the striatum: Implications for L-DOPA Induced Dyskinesia. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-02092018-155542/ ;

Chicago Manual of Style (16th Edition):

Warren, Emily Booth. “Mitochondrial dysfunction in the striatum: Implications for L-DOPA Induced Dyskinesia.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed December 07, 2019. http://etd.library.vanderbilt.edu/available/etd-02092018-155542/ ;.

MLA Handbook (7th Edition):

Warren, Emily Booth. “Mitochondrial dysfunction in the striatum: Implications for L-DOPA Induced Dyskinesia.” 2018. Web. 07 Dec 2019.

Vancouver:

Warren EB. Mitochondrial dysfunction in the striatum: Implications for L-DOPA Induced Dyskinesia. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2019 Dec 07]. Available from: http://etd.library.vanderbilt.edu/available/etd-02092018-155542/ ;.

Council of Science Editors:

Warren EB. Mitochondrial dysfunction in the striatum: Implications for L-DOPA Induced Dyskinesia. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://etd.library.vanderbilt.edu/available/etd-02092018-155542/ ;


Vanderbilt University

5. Hacker, Mallory Louise. Investigating the mechanism of GABA neuron degeneration in a model of coenzyme Q deficiency.

Degree: PhD, Cell and Developmental Biology, 2013, Vanderbilt University

 Neurodegenerative diseases are characterized by inappropriate death of distinct neuronal populations. Although symptoms vary, these diseases share pathogenic features such as age-dependent onset and progressive… (more)

Subjects/Keywords: apoptosis; mitochondria; C. elegans; Coenzyme Q; neurodegeneration; necrosis; GABA

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APA (6th Edition):

Hacker, M. L. (2013). Investigating the mechanism of GABA neuron degeneration in a model of coenzyme Q deficiency. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-07082013-073617/ ;

Chicago Manual of Style (16th Edition):

Hacker, Mallory Louise. “Investigating the mechanism of GABA neuron degeneration in a model of coenzyme Q deficiency.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed December 07, 2019. http://etd.library.vanderbilt.edu/available/etd-07082013-073617/ ;.

MLA Handbook (7th Edition):

Hacker, Mallory Louise. “Investigating the mechanism of GABA neuron degeneration in a model of coenzyme Q deficiency.” 2013. Web. 07 Dec 2019.

Vancouver:

Hacker ML. Investigating the mechanism of GABA neuron degeneration in a model of coenzyme Q deficiency. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2019 Dec 07]. Available from: http://etd.library.vanderbilt.edu/available/etd-07082013-073617/ ;.

Council of Science Editors:

Hacker ML. Investigating the mechanism of GABA neuron degeneration in a model of coenzyme Q deficiency. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://etd.library.vanderbilt.edu/available/etd-07082013-073617/ ;

6. Kraemer, Bradley Rhoads. A Role for the p75NTR in Axonal Degeneration and Apoptosis Induced by Oxidative Stress.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 The p75 Neurotrophin Receptor (p75NTR) is a critical regulator of axon pruning and apoptosis during neurodevelopment. Because the receptor has also been associated with many… (more)

Subjects/Keywords: neurotrophin; axon degeneration; p75NTR; apoptosis; oxidative stress

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APA (6th Edition):

Kraemer, B. R. (2014). A Role for the p75NTR in Axonal Degeneration and Apoptosis Induced by Oxidative Stress. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-08252014-160042/ ;

Chicago Manual of Style (16th Edition):

Kraemer, Bradley Rhoads. “A Role for the p75NTR in Axonal Degeneration and Apoptosis Induced by Oxidative Stress.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed December 07, 2019. http://etd.library.vanderbilt.edu/available/etd-08252014-160042/ ;.

MLA Handbook (7th Edition):

Kraemer, Bradley Rhoads. “A Role for the p75NTR in Axonal Degeneration and Apoptosis Induced by Oxidative Stress.” 2014. Web. 07 Dec 2019.

Vancouver:

Kraemer BR. A Role for the p75NTR in Axonal Degeneration and Apoptosis Induced by Oxidative Stress. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2019 Dec 07]. Available from: http://etd.library.vanderbilt.edu/available/etd-08252014-160042/ ;.

Council of Science Editors:

Kraemer BR. A Role for the p75NTR in Axonal Degeneration and Apoptosis Induced by Oxidative Stress. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://etd.library.vanderbilt.edu/available/etd-08252014-160042/ ;

7. Madison, Jennifer Lea. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.

Degree: PhD, Pharmacology, 2011, Vanderbilt University

 Huntingtonâs disease is a fatal autosomal dominant neurodegenerative disease caused by an expansion of CAG repeats in the DNA of the Huntingtin gene. The length… (more)

Subjects/Keywords: neuron morphology; YAC128; manganese; Huntington's disease; medium spiny neuron; neurochemistry

Aaron B. Bowman for taking me into their laboratories where I conducted my dissertation… …which I would not be where I am today. I came into graduate school at Vanderbilt University… …Environmental Engineering at Vanderbilt University for performing the ICP-MS analysis of striatal Mn… …Neurochemistry Core Lab at Vanderbilt University. The CMN/KC Neurochemistry Core Lab is supported by… 

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APA (6th Edition):

Madison, J. L. (2011). Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-06232011-150528/ ;

Chicago Manual of Style (16th Edition):

Madison, Jennifer Lea. “Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed December 07, 2019. http://etd.library.vanderbilt.edu/available/etd-06232011-150528/ ;.

MLA Handbook (7th Edition):

Madison, Jennifer Lea. “Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology.” 2011. Web. 07 Dec 2019.

Vancouver:

Madison JL. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2019 Dec 07]. Available from: http://etd.library.vanderbilt.edu/available/etd-06232011-150528/ ;.

Council of Science Editors:

Madison JL. Gene-environment interactions between mutant huntingtin and manganese exposure alter striatal neurochemistry and medium spiny neuron morphology. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://etd.library.vanderbilt.edu/available/etd-06232011-150528/ ;

8. Bylund, Jeffery B. BMP signaling regulation by GREMLIN 2 promotes proliferation and differentiation of human iPS cell-derived cardiac progenitors to cardiomyocytes.

Degree: PhD, Pharmacology, 2017, Vanderbilt University

 Heart development depends on coordinated proliferation and differentiation of cardiac progenitor cells, but how the two processes are synchronized is not well understood. The data… (more)

Subjects/Keywords: cardiomyocyte differentiation; human pluripotent stem cells; BMP signaling; GREMLIN 2

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APA (6th Edition):

Bylund, J. B. (2017). BMP signaling regulation by GREMLIN 2 promotes proliferation and differentiation of human iPS cell-derived cardiac progenitors to cardiomyocytes. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-03272017-212556/ ;

Chicago Manual of Style (16th Edition):

Bylund, Jeffery B. “BMP signaling regulation by GREMLIN 2 promotes proliferation and differentiation of human iPS cell-derived cardiac progenitors to cardiomyocytes.” 2017. Doctoral Dissertation, Vanderbilt University. Accessed December 07, 2019. http://etd.library.vanderbilt.edu/available/etd-03272017-212556/ ;.

MLA Handbook (7th Edition):

Bylund, Jeffery B. “BMP signaling regulation by GREMLIN 2 promotes proliferation and differentiation of human iPS cell-derived cardiac progenitors to cardiomyocytes.” 2017. Web. 07 Dec 2019.

Vancouver:

Bylund JB. BMP signaling regulation by GREMLIN 2 promotes proliferation and differentiation of human iPS cell-derived cardiac progenitors to cardiomyocytes. [Internet] [Doctoral dissertation]. Vanderbilt University; 2017. [cited 2019 Dec 07]. Available from: http://etd.library.vanderbilt.edu/available/etd-03272017-212556/ ;.

Council of Science Editors:

Bylund JB. BMP signaling regulation by GREMLIN 2 promotes proliferation and differentiation of human iPS cell-derived cardiac progenitors to cardiomyocytes. [Doctoral Dissertation]. Vanderbilt University; 2017. Available from: http://etd.library.vanderbilt.edu/available/etd-03272017-212556/ ;

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